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Overstretching alveolar epithelial type II cells decreases surfactant secretion via actin polymerization and intracellular trafficking alteration.
Inoue, Shigesato; Nagao, Junpei; Kawamoto, Kouhei; Kan-O, Keiko; Fukuyama, Satoru; Sasaki, Saori; Kudo, Susumu; Okamoto, Isamu; Sera, Toshihiro.
Afiliação
  • Inoue S; Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
  • Nagao J; Department of Mechanical Engineering, Graduate School of Engineering, Kyushu University, Fukuoka, Japan.
  • Kawamoto K; Department of Mechanical Engineering, Graduate School of Engineering, Kyushu University, Fukuoka, Japan.
  • Kan-O K; Department of Mechanical Engineering, Graduate School of Engineering, Kyushu University, Fukuoka, Japan.
  • Fukuyama S; Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
  • Sasaki S; Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
  • Kudo S; Department of Respiratory Medicine, National Hospital Organization Omuta National Hospital, Fukuoka, Japan.
  • Okamoto I; Department of Mechanical Engineering, Faculty of Engineering, Kyushu University, Fukuoka, Japan.
  • Sera T; Department of Mechanical Engineering, Faculty of Engineering, Kyushu University, Fukuoka, Japan.
Heliyon ; 10(13): e33499, 2024 Jul 15.
Article em En | MEDLINE | ID: mdl-39040228
ABSTRACT
Pulmonary surfactant is essential for maintaining proper lung function. Alveolar epithelial type II (AE2) cells secrete surfactants via lamellar bodies (LBs). In tidal loading during each breath, the physiological cyclic stretching of AE2 cells promotes surfactant secretion. Excessive stretching inhibits surfactant secretion, which is considered to contribute to the development of lung damage. However, its precise mechanism remains unknown. This study tested whether actin polymerization and intracellular transport are required for pulmonary surfactant secretion and the association of actin polymerization and transport in identical human AE2-derived A549 cells using live-cell imaging, not in the bulk cells population. We found that overstretching approximately doubled actin polymerization into filaments (F-actin) and suppressed LB secretion by half in the fluorescent area ratio, compared with physiological stretching (F-actin 1.495 vs 0.643 (P < 0.01); LB 0.739 vs 0.332 (P < 0.01)). An inhibitor of actin polymerization increased LB secretion. Intracellular tracking using fluorescent particles revealed that cyclic stretching shifted the particle motion perpendicularly to the direction of stretching according to the orientation of the F-actin (proportion of perpendicular axis motion prior particle 0h 40.12 % vs 2h 63.13 % (P < 0.01)), and particle motion was restricted over time in the cells subjected to overstretching, indicating that overstretching regulates intracellular transport dynamics (proportion of stop motion particle 0h 1.01 % vs 2h 11.04 % (P < 0.01)). These findings suggest that overstretching changes secretion through the cytoskeleton overstretching AE2 cells inhibits pulmonary surfactant secretion, at least through accelerating actin polymerization and decreasing intracellular trafficking, and the change in actin orientation would modulate intracellular trafficking.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2024 Tipo de documento: Article